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Available4.9
29 reviewsAbstractBackground: The mechanisms underlying volatile anaesthetic-induced unconsciousness remain unclear. Glutamatergicpyramidal neurones and fast-spiking interneurones in cerebral cortex circuits play distinct roles in cortical networkdynamics under volatile anaesthesia. We investigated the roles of medial prefrontal cortex (mPFC) pyramidal and fastspiking interneurones in volatile anaesthetic-induced hypnosis.Methods: The electrophysiological properties of pyramidal and fast-spiking parvalbumin (PV+) neurones were exploredby in vivo multichannel recordings and in vitro patch-clamp electrophysiological recordings. Chemogenetic manipulationwas used to test the role of pyramidal neurones in the mPFC in volatile anaesthetic-induced unconsciousness. Nav1.1knockdown in PV+ neurones was used to regulate activities of pyramidal neurones by PV+-dependent disinhibition andto investigate the role of pyramidal neurone activation in volatile anaesthetic-induced unconsciousness.Results: Regular-spiking pyramidal neurones and fast-spiking PV+ neurones in the mPFC were identified with distinctspiking properties. Sevoflurane suppressed pyramidal neurone firing frequency and action potential characteristics.Chemogenetic inhibition of pyramidal neurones in the mPFC enhanced the potency of volatile anaesthetics, whereaschemogenetic activation produced the opposite results. Sevoflurane also suppressed the firing of fast-spiking PV+neurones, with a greater inhibition ratio than that in regular pyramidal neurones; however, sevoflurane did not affect theaction potential properties of PV+ neurones. Nav1.1 knockdown in PV+ neurones enhanced sevoflurane-mediated suppression of PV+ neurone activity, leading to pyramidal neurone disinhibition and reduced hypnotic potency.Conclusion: The excitability of pyramidal neurones in the mPFC primarily determines the sedative potency of volatileanaesthetics in mice.Keyword
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